Upregulation of neuronal nicotinic receptor subunits α4, β2, and α7 in transgenic mice overexpressing human acetylcholinesterase

Marie M. Svedberg*, Anne Lie Svensson, Mary Johnson, Mandy Lee, Osnat Cohen, Jennifer Court, Hermona Soreq, Elaine Perry, Agneta Nordberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Neuronal nicotinic receptor binding sites as well as mRNA levels encoding for subunits α4, β2, and α7 were analysed in 3-mo-old transgenic mice generated with a neuronal overexpression of human acetylcholinesterase and in age-matched controls. The acetylcholinesterase transgenic mice display progressive cognitive impairment in spatial learning and memory. We here report a significantly increased [3H]epibatidine and [125I]αbungarotoxin binding in the cortex and the caudate putamen of these mice. Quantitative in situ hybridization showed significant upregulation of mRNA corresponding to the nicotinic receptor subunits α4, β2, and α7 in various brain regions in the transgenic mice compared to nontransgenic controls. Our results suggest that disruption of balanced cholinergic transmission by constitutive overexpression of acetylcholinesterase is accompanied by variable upregulation of several nicotinic receptor subtypes, in particular these associated with cholinergic terminals participating in compensatory response.

Original languageEnglish
Pages (from-to)211-222
Number of pages12
JournalJournal of Molecular Neuroscience
Volume18
Issue number3
DOIs
StatePublished - 2002

Keywords

  • Acetylcholinesterase
  • Acetylcholinesterase overexpressing mice
  • Binding sites
  • Cholinergic receptor
  • mRNA
  • Nicotinic receptors

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